Thrombolytic therapy is the specific therapy for Ischemic stroke , when administered in less than 3 hours ( Now 6 h ?) and has proven to save lives and brain .The only issue is , we need a 100% exclusion of hemorrhagic stroke by a CT/MRI. The mechanism of action of thrombolytic agent is simple .It lyses cerebral thrombosis and makes way for sustained reperfusion and arrest or even reverse the ischemic damage to neurones .

And now , let us see , how we perceive the same therapy in a patient with a history of recent ischemic stroke with an acute STEMI .

The issue is two fold.

He needs urgent myocardial salvage in the form of thrombolysis or PCI .

The thrombolysis or PCI should not worsen the cerebral infarct.

According to most standard literature thrombolytic therapy is an absolute contraindication in a patient with STEMI and recent history of ischemic stroke (<3 months )

The term absolute means ‘it is medical crime” to give TPA or Streptokinase.

How is it possible when the same drug is projected a savior in acute ischemic neurological emergencies and be dangerous when administered few months later in an evolved ischemic stroke ?

The major reasoning against thrombolysis in recent stroke is the potential concern for converting an indolent ischemic infarct into hemorrhagic infarct in a patient who may start bleeding into brain.

This is highly conjectural , as a previous history of ischemic stroke in no way increases the bleeding risk .Conversion of ischemic to hemorrhagic infarct tend to occur in the very early hours of acute stroke (not weeks later) .This could be part of calcium induced reperfusion injury .

Unanswered questions

The issue become further complicated with our skewed thinking pattern.

If thrombolysis is contraindicated in STEMI , does it any way imply a automatic indication for primary PCI ?

It seems so , for most of us !

How safe is PCI in a patient with a previous history of ischemic stroke ?

An emergency PCI in a patient who is expected to have widespread cerebral carotid , and peripheral vascular disease is fraught with added hazard.

The drug we administer during PCI are not innocuous ones . Aspirin , Heparin, clopidogrel (sometimes even 2b 3a!) will keep the risk of converting the ischemic infarct into hemorrhagic infarct remain at dangerous levels . This ridicules the very logic of PCI being preferred over thrombolysis in such situations .

So it is not an easy decision to do primary PCI in an elderly patient with STEMI and a recent CVA. It is only a mirage of medical intellectualism and the blind following of unscrutinized scientific literature that determine many of the decision making in cardiology .

The argument here is , in a patient with evolved , uncomplicated ischemic stroke thrombolysis can safely be administered irrespective of the age of stroke. .This is contrary to the published literature.Let us not make unethical practice against scientific literature but let us also understand it is unethical not to realise many of the so-called scientific evidence are merely speculative.I request the neurologists and cardiologists give their input on the issue

As far as I have searched the superiority or inferiority of thrombolysis vs PCI in recent ischemic CVA has never been compared one to one. The fact may be , such a study is never possible in the future .But it seems PCI has won the trial without a trial .

Unanswered questions

How many deaths have happened due to worsening of stroke after thrombolysis ?

How safe is a combination of aspirin, heparin and clopidogrel in a patient with recent stroke ?

How shall we decide about thrombolysis in these situations of STEMI and recent CVA) depending upon the

Age of CVA

Location of cerebral infarct

Size of the infarct

Residual neurological deficit

It may be prudent to redefine the indication for thrombolysis and PCI in a patient with history of recent or remote stroke.

It is logical to assess the potential risk of converting the ischemic cerebral infarct into hemorrhagic infarct.

It is expected only large infarct in vital locations need to be feared upon for this complication

All small healed cerebral infarct need not be worried about reactivation.

How to asses the healing of cerebral infarct?

The healing and gliosis is highly dependent on individual response to inflammation. Some heal within weeks. Neo vascularisation within the necrtoic area may get hyperpermiable .These are very speculative concerns. In all probability the risk of converting an ischemic necrosis into hemorrhagic necrosis is less than a percentage .The 3 months time for fixed for infarct healing is an arbitrary one

How good is MRI to predict a healed infarct from nonhealed infarct ?

As of now, we have no good tools to identify the safe infarcts that can withstand intensive anticoagulation or even thrombolysis .If the imaging techniques improve we may able to predict complete gliosis and the vascularisation of cerebral scars.

Post blog query

How to manage an elderly man with STEMI in a patient with recent ischemic stroke ?

A.Take him to cath lab and do primary PCI
B.Thrombolyse with TPA or Streptokinase
C.Just observe and manage with Heparin*

Answer : Any of the above can be correct answer .

If we still think the answer is only “A” great reforms need to be done in medical science . . .

*Another important option for STEMI and recent stroke (Perceived as inferior form of management of STEMI !)

An important option is , neither thrombolysis nor PCI just simple heparin for STEMI in these high risk individuals .This simple treatment has saved many lives .

In this world of gross approximation and perceived fears , it may be reasonable to shift the indication of thrombolysis for STEMI( with h/o recent stroke ) from absolute to relative contraindication.

Many of the junior physicians in the learning curve may take it as granted in the management of STEMI “If thrombolysis is contraindicated , then primary PCI must be indicated ” This again is absolutely not true !

Thrombus formation and subsequent lysis either spontaneous or pharmacological is the key events in acute vascular emergencies .We know both STEMI and acute strokes can get aborted naturally.

The thrombus which initially forms , triggers a natural lytic mechanism and this fights vigorously against the clotting process , and tries to get rid of the intravascular clot.

The early minutes are vital. (Like the T 20 cricket ) the win or loss is decided in the first few overs . The mantra is unrelented attack of the ball . . .ie thrombus ! In some patients the clot can never grow big to fill the lumen.These are lucky few .The mechanisms are common in both cerebral and coronary circulation. Here is were comes the role of antiplatelet agesnt .An aspirin or clopidogrel administered within minutes can prevent the genesis of central core of the thrombus .(This is the secret of aspirin scoring over stretokinase in STEMI in ISIS2 study done three deaceds ago !)

It should be realised, our understanding about spontaneous lysis is very little considering explosive growth of other aspects of cardiology. It is mediated by circulating TPA and antithrombin 3 . Remember every humans have it in their blood .But how much ? How to augment it ‘s power at times of thrombotic crises ?

The greatest adverse effect of modern medical science is the notorious phenomenon of amplifying medical trivia .We rarely realise how much of anxiety this causes to our patients. We can’t complain either, as many of the medical professionals make a living out this.

For cardiologists and echocardiologists , there is often an issue in reporting some of their findings .Doppler is a great tool , especially the color Doppler which can pickup even few clusters of RBCs that leak into atria every time the AV valves closes. Ideally this has to be labeled as physiological MR or TR .If the arotic root is obliquely aligned with it’s leaflets one may even get a physiological AR .

While it is better to ignore these lesions , some call it as Trivial MR / TR/AR .

This can be detected up to 40 % of individuals.

What does trivial regurgitation mean to a doctor ?

It means nothing . Few may use it as a weapon to advice further visits to their clinic and do serial meaningless follow up scans .The irony is some of these patients enjoy this . . . and it becomes a different matter altogether.

What does it mean to the patient?

Anxiety for the majority , for the modern net educated public. No issue , for the ignorant and the take it easy men ! We have seen number of patients getting cardiac symptoms after reporting the physiological MR or TR.

So, should we report physiological events in routine echocardiogrpahy?

We need not . But we do it often .Why ?

There are few reasons for this phenomenon ( Which I believe are true , after observing as many echocardiography centers for more than few decades)

Doctors and Imageologist are often self suspicious and worried about missing something and getting exposed among their peers and public. They do not want to miss any abnormality. So even a trival abnormality of negligible importance is also reported.

In the prevailing Geo commercial medical world there are issues other than academic creeping in..

Many get bored to report normal reports as they want to add spice to their report hence they fill it up all fancy terminologies . This sort of spice reporting adds self esteem the medical professionals .It makes some sense to report and reveal what they know to the non specialists.

Finally, the present day high IQ patients also do not expect a bland ( normal ) report.They often relish some scribblings in their master health check reports. They tend to question the authenticity if we simply say everything is normal.

The following can be termed as Echo trivia in otherwise healthy individual

Mild LVH

Age related impaired relaxation of LV without LA enlargement.

Mitral valve prolapse without MR

Minimal pericardial effusion

Patent foramen ovale without any shunting

When does a trivial lesions can be important ?

In a patient with established heart disease , a trivial valve leak could become important. For example in dilated cardiomyopathy, COPD, MVPS dilated aortic root etc .Here regular follow ups may be necessary.

Aortic and mitral valve degeneration with calcification in the elderly is now implicated in many of the unexplained strokes .Hence even though it is age related physiology it need to be given importance.

Can trivial regurgitant lesions be a risk for infective endocarditis.?

No one knows. Logic would imply a risk , as micro jets are the norm here . But the potential for it to cause a endothelial damage is negligible. Some sinister thinking cardiologists Many of the native valve endocarditis in otherwise normal hearts may be attributed to this physiological MR/TR .(Evidence less cardiology !)

Chest pain as a symptom in acute MI is vitally important as it only brings the patient to the ER. (Realise ,silent MIs can never reach the hospital in time ! ). Heart is located few centimeters beneath the chest wall and extend up to 15 cm posteriorly.The location heart within the chest wall , make it a three dimensional structure .Theoretically pain can initiate in one focus and radiate to any direction. Traditionally , when we say chest pain , we mean the anterior chest wall on either side .Technically , chest contains a lateral and a posterior wall .The posterior surface of the chest is called back of chest , or some times simply the back .

We know , chest pain can radiate to many sites , of course the much hyped (May not be common yet !) being the radiation to left shoulder , and arm.

The ischemic chest pain , even though described as classical angina over a century ago . It applies mainly to stable exertional angina .In STEMI or unstable angina these rules are can not be expected to be followed strictly.

We often think the pain of MI comes only from the myocardium , but there are many potential sources

The adjacent pericardium

coronary artery dissection, plaque fissures

Neuralgic pain from the ischemic nerve terminals

Finally dermatomal reference pain

What is the quantum of pain signals arise from each of these components ? Obviously , myocardial pain should be the dominant one .Here again , there is a dichotomy .Whether the infarct segment elicits more pain or the surrounding ischemic segment is also not clear. The is an important difference the character of pain infarct pain is a severe continuous dull aching .Some believe in a fully infarcted segment where the nerve terminals are dead can not carry pain signals and pain is absent, while partially dead muscle produce maximum pain.

The somatic nervous system , that mirrors the visceral pain into the dermatomes that the patient feels as if the pain is originating from these sites. Heart is a huge middle mediastinal structure , primarily reflects the pain to the anterior chest wall , but no surprise if it deflects the pain signals posteriorly also. Of course , the spine and the thick posterior chest muscle walls tend to block this transmission.

But , on many occasions patient who are admitted with ACS in CCU complain pain in the back of chest

the following things has been observed.

Severe back pain in a patient with large STEMI invariably indicate a myocardial tear .

Mesentric and coeliac artery occlusion

Aortic dissection

Back pain only STEMI

Every cardiologists would have seen atleast few cases of STEMI presenting only as back pain.The problem here is they land up in varied departments .We have on instance of a STEMI landing to a ortho surgeon .He was good enough to suggest an ECG and that showed an extensive infero posterior MI and later shifted to coronary care unit.

Back pain as marker of impending rupture

Severe back pain in an established STEMI is a ominous sign as it is often a marker of impending rupture. Here the patient is in extreme distress, and may become violent and restless .(Hypoxia adds to woes!)

Does posterior MI more likely to produce back pain or posterior chest pain ?

Not proven but distinctly possible. ( posterior MI -Posterior pericarditis- Back pain .)We emphasize posterior chest leads in ECG V7 to V10 in inferoposterior MI . We expect the injury current to flow to the back , is it not logical some of the neural signals would also reach the back.

Final message

Never underestimate back pain. We are tuned to think chest has only one surface that is anterior .This is a gross missense .After all , there is a huge area(> 30X 30 cm ) of chest wall located behind us .

Take an ECG in all patients with acute pain in the back of the chest . Even though this may look a funny advice . . . it is an important clinical tip for all those budding physicians of this world. If one life is saved per 100 innocent back pain cases , this article acheives it’s purpose !

Technically and literally it means a “Take it easy attitude” as long as patient is comfortable , even a rate of more than 100 is allowed . Few years back the above concept could be termed a “non sense”

Final message

In this perennial management issue of AF , Whether , we were successful in restoring sinus rhythm or not , we have restored the common sense* Thanks to RACE 2 investigators.

* Do not unnecessarily trouble a asymptomatic patient with those powerful and costly antiarrhythmic drugs .